Evidence from previous work suggests that the 'automatic' component of respiratory control is either inadequately stimulated or activity inhibited in the sheep fetus and is then activated at birth. We are studying the nature of this inhibition. We are first studying how it is that the carotid body chemoreceptors are inactive in the fetus and also the nature of the transducer mechanism of these receptors in the adult cat. We are studying the nature of central chemosensitivity in the fetus by (a) infusing buffers of varying pH into the cerebral ventricles and (b) by raising fetal venous and arterial Pco2 by infusing CO2 into the peritoneal cavity. We have been able to show that respiratory sensitivity to CO2 is considerably less in the fetus than in the newborn lamb and that respiratory activity is very difficult to induce in the periods of apnea. Measurement of evoked potentials in the fetal somato-sensory cortex indicates that during the periods of apnea, conduction is normal whereas these potentials are effectively abolished during periods of respiratory activity suggestive of REM sleep. The apnea does not therefore appear to be due to inhibition of afferent somatic activity. Measurements of the distribution of cerebral glucose utilization show that in the fetus respiratory activity is associated with an increase in both hypothalamus and nucleus of the solitary tract and that at birth, there is an increase in glucose utilization in virtually every part of the brain. In the newborn infant and newborn lamb, recordings of respiratory traces in designated sleep states show that there is a well-marked maturation of the respiratory responses to spontaneous or induced disturbances to respiration suggesting increasing maturity of the 'automatic' control of respiration.